PICU Primer I

Kevin M. Creamer M.D.

Pediatric Critical Care Walter Reed AMC

The Primer Outline

 Physiology – Hypoxia / Hypoxemia – ABG’s and Acidosis – Sodium and H 2 O metabolism – Hemodynamics and Cardiopulmonary interactions  ICU Care & Common Problems – Head trauma – Toxicology – Postoperative issues – Mechanical Ventilation

Can you have hypoxia without hypoxemia?

Can you have hypoxemia without hypoxia?

Oxygen and Hypoxemia

 Define – Hypoxemia – Hypoxia

Hypoxemia

 Ventilation/Perfusion mismatch  Hypoventilation  Shunt  Diffusion  Decreased Ambient O 2

Oxyhemoglobin Curve

>> low pH, high Temp

Shunt / Dead Space Spectrum

Shunt Dead Space V/Q = 0 V/Q = infinity

No amount of  O 2  difference will fix between EtCO 2 and PaCO 2

Ventilation / Perfusion mismatch

V  Blood  Pus  Air  Water  Atalectasis

Q >>>

 Quantitate using A – a Gradient

A – a Gradient

(P b -P H2O ) x FIO 2 - (PCO 2 /.8) - PaO 2

 Other useful equations – Dead Space = 1 - (EtCO 2 /PaCO 2 ) –

OI = (P aw x FIO 2 x 100)/ PaO 2

• Positive vs. negative pressure

Cause for desaturations

 Anesthesia – hypoventilation  Atalectasis – V/Q mismatch  Edema - V/Q mismatch  Asthma– dead space/ V/Q mismatch  Dysfunctional Hemoglobin  You may need a CXR and or ABG in addition to H+P to answer the question

Non respiratory Physiologic causes of a low PaO 2 Causes Effect on P(Aa)O 2 Nonrespiratory Righttoleft intracardiac shunt Decreased PIO 2 Low barometric pressure Low FIO 2 Decreased R value Low mixed venous oxygen content* Artifact Very high white blood cell count Patient hyperthermia Increased Normal Normal Increased Increased Increased

*Only in presence of increased venous admixture

Hypoxia

 Hypoxic - ex. pulmonary disease  Anemic – ex. low CaO 2 , CO poisoning  Distributive - ex. sepsis, emboli  Histotoxic – ex. cyanide

Oxygen Debt/ Oxygen Deficit

45 40 35 30 O2 in ml 25 20 15 10 5 0 10

MODS > Death >?

Inadequate Resuscitation

20 30 40 Time (minutes) 50 60 O2 Deficit O2 Debt

Oxygen Content

 Which has the biggest impact on O 2 delivery to the tissues?

– Hemoglobin, Sat, Cardiac Output, or PaO 2  Which patient has more oxygen in the blood?

– Patient A, PaO 2 89, Sat% 97%, Hg 9.8

– Patient B, PaO 2 60, Sat% 85%, Hg 13.1

V A

20 15 10

Hb 15 // Hb 10 Hb 7.5

// // Hb 0 //

PO2 25 50 75 100 150 600 Sat% 50 75 90 99 100

Preload HR Contractility Afterload SV

Hg

PaO 2 Sat % CO CaO 2 DO 2

“Normal” Values

 CaO 2 (PaO 2 = (Hg X 1.34 X Sat%) + X 0.003) – 17-20cc O 2 /dL  DO 2 = CI X CaO 2 – 400-600 ml X min / M 2 Arterial sat 100% minus  VO 2 = CI X avDo 2 – 140-160 ml X min / M 2 Consumption = Venous sat 75-80%

Oxygen Rules of Thumb

 Give enough – high flow non-rebreather if needed  Look for a reason for low Saturations – Postop Posterior Spinal Fusion Pt with Sats 88%  Don’t be fooled by a little – 5 kg baby , RR 40, I:E 1:2, on 2L NC – What’s the FiO 2 ?

Questions?

 NEXT UP – ABG’s and acidosis

Acidosis

 Respiratory vs. Metabolic?

– Anion gap or not?

 Acute vs. Chronic?

 Primary or Secondary?

 Rule – every 10 torr change in PCO 2 0.08 change in pH should result in – Every HCO 3 drop you should see 1:1 increase in base excess

ABG quiz

A B C D

pH

7.15

7.35

7.45

7.20

PCO 2

25 56 34 60

PO 2

93 71 95 55

HCO 3

8 31 25 20

BE

-13 +5 0 -4

Sat

99% 96% 99% 87% 1. 1° Respiratory Alkalosis 2. 1° Respiratory and 1° metabolic acidosis 3. 1° Resp acidosis and 2° Metabolic alkalosis 4. 1° Metabolic acidosis and 2° Resp alkalosis

ABG quiz

A B C D

pH

7.15

7.35

7.45

7.20

PCO 2

25 56 34 60

PO 2

93 71 95 55

HCO 3

8 31 25 20

BE

-13 +5 0 -4 1. Crying healthy infant 2. Former preemie with bad BPD 3. Salicylate toxicity 4. Postop spinal fusion patient 5. Moderate Asthma attack on O 2 6. DKA

Sat

99% 96% 99% 87%

Acidosis - Anion Gap?

 Pay attention to the frequently overlooked HCO 3 on the Chem-7 – It’s measured not calculated  Does the Chloride rise as the HCO 3 drops?

Acidosis - Osmole Gap ?

 IF AG is + then calculate the osmole gap – Difference between measured and calculated OSMs – Osm = 2(Na + ) + BUN/2.8 +Glu/18

Anion Gap vs. Non Anion Gap

      

M U D P I L

ethanol remia KA araldehyde ron/INH/inhale CO actic Acid

E

thanol/Ethylene Glycol 

S

alicylates  GI HCO 3 losses  Renal tubular acidosis  Carbonic Anhydrase inhibition  TPN?

 Hypoaldosteronism

Metabolic Acidosis Normal Gap Potassium?

Hypokalemia Nl/Hyperkalemia Elevated Gap Nl Osm Gap OSM Gap?

Elevated Osm Gap RTA I,II Diarrhea RTA IV Hypoaldosteronism M UDPIL E S Ethylene gylcol Ethanol Methanol

Acidosis treatment

 Correct underlying problem – restore perfusion !!!

 NaHCO 3 usually not necessary – Paradoxical CNS acidosis – Left shift of oxyhemoglobin curve  Think about funky metabolic disorders if the story doesn’t fit

Funky Acidosis Workup

 First 1-2 hours – ABG – Chem 10 – Lactate – Ammonia – Ketones – Urinalysis – consider CBC and LFTs’

Questions?

 NEXT UP – Sodium and water metabolism  “There is no such thing as free water, sooner or later you have to pay for it”

Sodium and Water H+P

 HX- intake, output of water and salt – Ex. (V/D) , boiled milk or home-made solutions  Intravascular Volume (Hi, Low, Nl)  Urine volume and concentration  Renal Fxn – BUN, Cr, K + – FeNa + = (UNa + /PNa + )

/

(Ucr/PCr) • <1% Low effective ECF

Hypernatremia

Diagnosis

Urine SpGr

Hypertonic Dehydration Diabetes Insipidus

Concentrated Dilute Low Intravascular Volume Sodium intake Low Normal Normal

Salt Poisoning

Normal Normal / Low High Common in under watered ICU patients

Hypernatremia - Other

 DI – Central - responds to ADH • look for a CNS lesion – Nephrogenic - doesn’t respond to ADH  Don’t forget – Mineralocorticoid Excess – Renal d/o with High PRA

Treatment

 Goal of any hyperosmolar state correction is to fix problem while avoiding cerebral edema – Pesky idiogenic osmoles  correct over 48 hours  Hypertonic state may mask symptoms  Correct both Na + and H 2 O deficits

Treatment

 Correct at rate 0.5-.75 mEq/L/hr  Check lytes q4-6°  Watch for Hypogylcemia, Hypocalcemia If Na + < 160 Fluid = 1/2 NS

If Na + > 160Fluid = NS

 Assume all losses are 140 meq/L Na +

Hypernatremia Example

10 d.o. 3.3 kg patient presents with Na + Birth wt 3.9 Kg – assume 600 cc lost is all 140 meq/L Na + – add daily Na + and H 2 O X 2 – calculations yield 1/2 NS at 28cc/hr 172,

* remember rule and use NS

USE NS and make the patient NPO for at least the first 12 hours

Hyponatremia

 Pseudohyponatremia? i.e. DKA  Volume status?

–

High

- CHF, Renal or Liver failure, hypoalbuminemia –

Normal

- excess free H 2 O intake, or SIADH, hypothyroidism –

Low

- GI, Skin,CSF or tissue losses, diuretics, CSW, adrenal insufficiency

Volume Status Serum Sodium Urine Sodium Urine volume Net Sodium loss SIADH CSW         ± 

Hyponatremia

 Checking urine sodium is invaluable  Remember iatrogenic losses – Drains • Lumbar, or JP, etc – Lasix • hyponatremic, hypokalemic, metabolic alkalosis • fix by replacing Cl , not Na + • give KCL

Treatment

 One goal of hyponatremia correction is to avoid Central Pontine Myelinolysis  Correct both Na + and H 2 O deficits  Correct at rate 0.5 mEq/L/hr  Treat Shock with NS then fix other deficits more slowly

Special Situations

 SIADH – Restrict free H 2 O • 3/4 maintenance NS – 3% Saline only for seizures • push 2-4 ml/kg over 5 -10 minutes until seizure stops – Lasix isn’t going to work  CSW – Replace ongoing Na + and H 2 O losses with combination of 3% and NS

Questions?

 NEXT UP – Hemodynamics and Cardiopulmonary interactions  Pop quiz –

What are the five determinants of Cardiac output??

Hemodynamic Determinants

 CO = HR X SV –

Preload

–

Afterload

-Volume -Resistance to LV emptying –

Contractility

–

Heart Rate

–

Rhythm

-Squeeze  rate =  SV -Atrial kick 10% CO  Ohm’s Law(V= I X R) or

BP = CO X SVR

Hemodynamic Determinants

Blood Pressure Stroke volume Contractility Preload Cardiac output Systemic vascular resistance Heart Rate Afterload

Cardiac output I

 Pulse quality  Central vs. Peripheral pulses  Differential Temperatures  Capillary refill time (CRT)  Organ Perfusion • CNS - AVPU?

• Renal - UOP – only organ with easily measured output  Acidosis?

Hemodynamic Assessment

 Stroke volume - pulse quality  Preload -

Liver size

, CXR - heart size  SVR - CRT, Pulse pressure, differential temperatures

Altered Hemodynamics

 Common features – Elevated HR - attempt to  CO – Elevated RR - beware Resp. alkalosis – Decreased pulses  CO – Depressed LOC  CO – Acidosis  CO – Falling UOP  CO

Distinguishing Exam

Scenario

Hypovolemic

Signs

WOB CRT Liver nl >2 nl Skin Cool Cardiogenic +++ >2 +++ Cool Distributive +/++ +/ nl +/-

Preload

Treatment priorities

Contractility Afterload

Cardiopulmonary Interactions

 Heart and Lungs intimately linked especially during critical illness – Ex. Valsalva can cause which results in   intrathoracic pressure in CO via  venous return – RV filling inversely proportional to Thoracic pressure  Spectrum – Pulsus paradoxicus PEA 2° Tension pneumo Too much

-

Too much

+

Cardiopulmonary Interactions

 Influence of negative pressure ventilation on healthy hearts is negligible  Normally systemic venous return is the main determinant of CO  Lung volume or (stretch) can PVR

Lung volume

PVR FRC

Cardiopulmonary Interactions

_ _ _ _ _

Negative pressure ventilation

Normal Disease

Right Preload   PVR

_

  Left Afterload +/ 

Cardiopulmonary Interactions

+ + + + +

Positive pressure ventilation Health Disease Right Preload    PVR

+

   Left Afterload +/ 

Cardiopulmonary Interactions

 4yo with febrile pneumonia, pleural effusions, poor PO intake and decreased UOP needs endotracheal intubation for respiratory failure – What is going to happen when you intubate?

 Be wary of over stretch in infants – Hyperinflation >>  vagal tone >> bradycardia and vasodilation

The End

Mind what you have learned. Save you it can.

Questions?